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There were no significant differences in baseline characteristics

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The main mechanism of NE inactivation is its presynaptic reuptake via a selective NE transporter, followed by metabolism by monoamine oxidase A (MAO A) and catechol-O-methyltransferase (COMT), with formation of 3-methoxy-4-hydroxyphenylglycol (MHPG), measurable in CSF

DEXA administration was shown to stimulate the development of IR [10,11,12,13] and NAFLD in numerous reports [9, 14, 41]